Table 2. Evidence summary of nutritional interventions on feeding behavior and metabolic outcomes

Intervention category	Example	Model system	Key findings	Primary mechanisms	References
Prebiotics (inulin)	Inulin-type fructans	Overweight/obese humans (meta-analysis)	↓Body weight (1-2 kg)↓Fat mass↑Satiety	↑Bifidobacterium↑SCFA production↑GLP-1, PYY secretion	Beserra et al., 2015
Prebiotics (propionate ester)	Inulin-propionate ester	Overweight adults (RCT)	↓Energy intakePrevention of weight gain↓Reward brain activation	↑Colonic propionate↑PYY secretionAltered brain processing	Chambers et al., 2015
Prebiotic (GOS)	Galacto-oligosaccharides	Human adults (RCT)	↓Cortisol response↓Anxiety in IBS patients↑Bifidobacterium	↑SCFA productionHPA axis modulationMicrobiota shifts	Schmidt et al., 2015
Resistant starch	RS2/RS3	Human adults (systematic review)	↓Postprandial insulin↑Insulin sensitivity↑Satiety	↑Butyrate production↑GLP-1 secretionImproved glucose metabolism	Bodinham et al., 2010
Postbiotics	Butyrate	Low-fat & high-fat diet mice	Cohort-dependent metabolic effectsVariable glucose toleranceMicrobiota-associated responsiveness	Context-dependent SCFA signalingBaseline microbiota determines efficacy	Lee et al., 2018
Probiotics	Encapsulated probiotics	High-fat diet rats	↑Barrier function↓InflammationImproved glucose metabolismEnhanced vs. non-encapsulated	↑Intestinal delivery↑Colonization↓Metabolic endotoxemia	Heo et al., 2019;Lee et al., 2020
Next-generation probiotics	PasteurizedA. muciniphila	Overweight/obese humans (RCT)	↓Insulin resistance↓Total cholesterol↓Liver dysfunction markersImproved barrier function	↑Mucus layer↓Metabolic endotoxemiaImmune modulation	Depommier et al., 2019
Functional foods	Goji berry	High-fat diet mice	↑Intestinal integrity↓Inflammatory profilesImproved gut microbiota↓Body weight gain	Prebiotic polysaccharidesAnti-inflammatory polyphenolsMicrobiota modulation	Jeong et al., 2024

[Note] The evidence summarized in this table spans preclinical studies, randomized controlled trials (RCTs), and meta-analyses, with greater interpretative weight given to human studies for clinical relevance. Preclinical findings were used primarily to support mechanistic understanding. Feeding behavior–related outcomes were interpreted based on their directness, with energy intake and satiety measures considered primary endpoints, followed by body weight/composition and metabolic markers as downstream outcomes. Stronger evidence for feeding behavior modulation was inferred when consistent effects were observed across multiple endpoint categories.